Electrolyte abnormalities Flashcards
Diabetes insipidus (DI).
a) Two main types and causes of each
b) Clinical features
c) Investigations
d) Management
e) Differentiating DI from primary polydipsia
a) Cranial.
- mechanism: inadequate production of ADH
- causes: idiopathic, head injury, pituitary tumour or surgery, hypothalamic dysfunction, Sheehans syndrome, inflammation (eg. sarcoid, GBS)
Nephrogenic
- mechanism: defect in AQP channels/ V2 receptors
- causes: CKD, lithium, hypercalcaemia, inherited
b) Polyuria, polydipsia, dehydration, hypernatraemia, raised serum osmolality and reduced urine osmolality
c) - Urine: osmolality, dip (?glucose)
- Bloods: serum osmolality, U+Es, glucose, calcium (differential - hypercalcaemia)
- Water deprivation test (shows inadequate concentration of urine)
- Then add desmopressin to distinguish cranial from nephrogenic DI (cranial: AVP leads to urine concentration)
- If cranial cause suspected - MRI pituitary/hypothalamus
d) Cranial - desmopressin nasal spray or tablets
Nephrogenic - conservative? - increase fluid intake
e) Primary (psychogenic) polydipsia - patients are able to concentrate their urine on water deprivation testing (rise in urine Osm and reduction in serum Osm)
Requirements per day.
a) Sodium
b) Potassium
c) Water
d) Adequate urine output (per hour)
e) Glucose
a) 1 mmol/kg/day
b) 1 mmol/kg/day
c) 25 - 30 ml/kg/day (~ 1 ml/kg/hr)
d) > 0.5 ml/kg/hr (~ 30 - 40 ml/hr)
e) 50–100 g/day
-
-
Body fluid.
- 70 kg man (if 60% body mass is water), calculate:
a) Total body fluid (L)
b) Intracellular fluid (L)
c) Extracellular fluid (L) - split into interstitial and intravascular
70 kg man
x 0.6 = 42 L total body water
2/3 is intracellular = 28 L
1/3 is extracellular = 14 L
Of the extracellular,
- 75% is interstitial = 10 L
- 25% is intravascular = 4 L
Water balance: regulating mechanisms
Raised plasma osmolality:
- Detected by osmoreceptors in hypothalamus
- Thirst response - drink more water
- Vasopressin secreted by posterior pituitary
- Attaches to V2 receptors in collecting ducts of kidneys
- AQP-2 channel up-regulation in collecting ducts
- Increased water reabsorption (reduced excretion)
- Reduces plasma osmolality
Osmolality.
a) What is it? (units)
b) Equation
c) Normal range
a) Concentration of solute (mOsm) per kg of water
b) 2x [Na+] + urea + glucose
c) Normal Osmolality = 282 - 295 mOsmol/kg
d)
Osmolality.
a) High plasma, high urine
b) High plasma, low urine
c) Low plasma, high urine
d) Low plasma, low urine
a) Dehydration (hypernatraemic)
b) Diabetes inspidus (hypernatraemic)
c) SIADH (hyponatraemia)
d) Primary polydipsia, fluid overload (hyponatraemia)
Hyponatraemia: aetiology
- 3 distinctions, with main causes for each
- Hypovolaemic (dry, tachy, low BP, etc.)
- Low urinary Na+:
• Vomiting + diarrhoea
• Burns
• Pancreatitis
- High urinary Na+ (salt-wasting): • Diuretics • Addison’s (or occasionally pituitary failure) • Cerebral salt wasting • Salt wasting nephropathy
- Euvolaemic:
- Acute water load / primary polydipsia
- Hypothyroid
- SIADH
- Low glucocorticoid (non-salt wasting) - Hypervolaemic (raised JVP, oedema, etc.)
• Cirrhosis of liver/liver failure
• CCF
• CKD / nephrotic syndrome
Hyponatraemia: clinical features
a) Severity depends on what 2 factors?
b) Possible features
a) Speed of onset; severity of hyponatraemia
b) - asymptomatic, or…
- Mild: • headache, • lethargy, • anorexia and abdominal pain, • weakness, • confusion
- Severe: • delirium/hallucinations, • agitation • seizures • decreased conscious level • coma
Hyponatraemia: investigations
a) Urine
b) Blood
c) Special tests
d) If SIADH suspected - 2 Ix?
a) Urinary electrolytes (eg. sodium), osmolality, glucose, protein, cortisol
b) Plasma osmolality, glucose, U+Es, TSH, cortisol, LFTs
c) - If cortisol low - synacthen test
d) CXR and CT head (usually chest and brain causes)
Acute hyponatraemia: management
acute is < 24 hour duration
Rapid hypertonic saline replacement.
- Manage in HDU/ITU setting
- 150 ml of 3% NaCl given IV over 15 mins
- Repeat if no response
- Monitor U+Es, etc.
- Aim for no more than 10 mmol/L increase per 24 h
Chronic hyponatraemia: management (> 24 hour duration)
- general management
- Hypovolaemic vs. euvolaemic vs. hypervolaemic
- complication of replacing sodium too quickly
General management.
- stop any precipitants (eg. diuretics)
- Treat the underlying cause
Hypo.
- IV NaCl 0.9%
Euvolaemic/hyper.
- Fluid restrict
Complication of rapid correction.
- Central pontine myelinolysis - leads to quadriplegia, locked in syndrome, etc.
SIADH.
a) Causes
b) 3 criteria to diagnose
c) Clinical fx
d) Suspect in anyone with cancer who has what electrolyte abnormality?
e) Investigations and management
a) Mainly pulmonary, CNS, malignant and drug-induced causes. SIADH:
- Small cell lung cancer/other malignancy (eg brain mets)
- Infection (pneumonia, TB, HIV)
- (sub)Arachnoid haemorrhage (and other CNS - head injury, SOL, meningitis, GBS, MS)
- Drugs: diuretics, SSRIs, ACEIs, PPIs
- Hereditary (rare)
b) - Euvolaemic hyponatraemia
- Low serum osmolality and raised urine osmolality
- Normal thyroid and adrenal function
c) - Often asymptomatic
- Hyponatraemia: anorexia, headache, cramps, nausea, vomiting, lethargy. Severe: reduced GCS, seizures
d) Hyponatraemia
e) - Investigate for cause (if unknown): CT TAP / CT head
- Treat underlying cause
- 1st line: fluid restriction
- 2nd line: demeclocycline (blocks ADH and induces partial nephrogenic diabetes insipidus)
- 3rd line: vaptans (eg, tolvaptan): vasopressin V2 receptor antagonists
A 28 year old man has an road traffic accident, with severe head injury. Unconscious, blood noted in external auditory meatus. Wakes up very thirsty, and within 24 hours is producing 6 litres of urine/day
• Serum sodium 154mmol/l
a) Likely diagnosis
b) How is it differentiated from diabetes mellitus?
c) What other investigations would you do?
a) Diabetes insipidus (cranial)
b) No glycosuria, no hyperglycaemia
c) - Urine: dip, osmolality, collection (total urine output: will be > 3L in DI)
- Serum: osmolality, calcium, glucose, U+Es, LFTs
- Imaging: CT head/ ?MRI pituitary
- Special tests: water deprivation test (+ desmopressin)
Hypernatraemia.
a) Main causes
b) Clinical features
c) Investigations
d) Management - general
e) Specific in DI
a) - Dehydration - inadequate intake, thirst impairment (eg. dementia), excessive water loss
- Diabetes insipidus
- Inappropriate diuresis or laxatives
- Watery diarrhoea/ excessive sweating
b) - Dehydration: thirst (+ polyuria in DI), dry
- CNS: lethargy, weakness, confusion, irritability, myoclonic jerks, seizures, coma
c) - Urine: dipstick
- Blood: U+E, calcium, glucose
?lithium levels
- Urine and plasma osmolality if DI suspected
- ?CT head if DI suspected
d) - Treat underlying cause
- Stop any precipitants (eg. loop diuretics, osmotic laxatives)
- Correct imbalance using hypotonic saline (0.45% NaCl)
- If acute - rapid correction
- If chronic - slow correction
e) - Nephrogenic (increase fluids)
- Cranial (desmopressin nasal spray)
